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© Research
Publication : Journal of leukocyte biology

Novel function of STAT1beta in B cells: induction of cell death by a mechanism different from that of STAT1alpha

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of leukocyte biology - 11 Sep 2008

Najjar I, Schischmanoff PO, Baran-Marszak F, Deglesne PA, Youlyouz-Marfak I, Pampin M, Feuillard J, Bornkamm GW, Chelbi-Alix MK, Fagard R

Link to Pubmed [PMID] – 18753311

J. Leukoc. Biol. 2008 Dec;84(6):1604-12

Alternate splicing of STAT1 produces two isoforms: alpha, known as the active form, and beta, previously shown to act as a dominant-negative factor. Most studies have dealt with STAT1alpha, showing its involvement in cell growth control and cell death. To examine the specific function of either isoform in cell death, a naturally STAT1-deficient human B cell line was transfected to express STAT1alpha or STAT1beta. STAT1alpha, expressed alone, enhanced cell death, potentiated the fludarabine-induced apoptosis, and enhanced the nuclear location, the phosphorylation, and the transcriptional activity of p53. Unexpectedly, STAT1beta, expressed alone, induced cell death through a mechanism that was independent of the nuclear function of p53. Indeed, in STAT1beta-expressing B cells, p53 was strictly cytoplasmic where it formed clusters, and there was no induction of the transcriptional activity of p53. These data reveal a novel role of STAT1beta in programmed cell death, which is independent of p53.

https://www.ncbi.nlm.nih.gov/pubmed/18753311